04-12-2022, 09:18 AM
You can believe what you want Grayson, but your takeaway is DIM is a just an estrogen reducer that’s somehow related to tamoxifen...I don't where got that from that's incorrect. Yes, Tamoxifen and DIM are used in cancer research.
Judging by your comment you didn't look at the posted literature, too bad…I'll list for you again.
DlM improves estrogen metabolism,
DIM shifts production of the dangerous estrogen metabolite 16a-hydroxy in favor of the beneficial (or healthier) 2-hydroxy 2-OH metabolite. So it's hypothesized that the 2 OH pathway over 16α-OH pathway (which is inversely associated with breast cancer risk) is a safer option.
So tell me, can Spiro do all this?
Does Spiro significantly improve insulin resistance like DIM
DIM on human prostate cancer cell growth were examined using LNCaP and PC-3 cells.
Our results showed a concentration-dependent inhibition of DNA synthesis of these cells of up to 90% under both uninduced and androgen-induced growth conditions.
Spiro doesn't even come close to that (60-70% at best)
DIM suppresses cell proliferation of LNCaP cells and inhibits dihydrotestosterone (DHT) stimulation of DNA synthesis.
DIM inhibited androgen-induced androgen receptor (AR) translocation into the nucleus. Results of receptor binding assays indicated further that DIM is a strong competitive inhibitor of DHT binding to the AR.
In addition, DIM inhibited proliferation and induced programmed cell death in human breast tumor cells in culture (20, 21).
We found that DIM is a strong antiandrogen that inhibited androgen-dependent tumor cell growth and competitively inhibited androgen receptor translocation and signal transduction.
DIM disrupts AR function in a manner similar to a chemically dissimilar synthetic antiandrogen, Casodex (similar to Bicalutamide)
Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16alpha-hydroxyestrone ratio in premenopausal and postmenopausal women
P Muti et al. Epidemiology. 2000 Nov.
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Abstract
Experimental and clinical evidence suggests that 16alpha-hydroxylated estrogen metabolites, biologically strong estrogens, are associated with breast cancer risk, while 2-hydroxylated metabolites, with lower estrogenic activity, are weakly related to this disease. This study analyzes the association of breast cancer risk with estrogen metabolism, expressed as the ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone, in a prospective nested case-control study. Between 1987 and 1992, 10,786 women (ages 35-69 years) were recruited to a prospective study on breast cancer in Italy, the "Hormones and Diet in the Etiology of Breast Cancer" (ORDET) study. Women with a history of cancer and women on hormone therapy were excluded at baseline. At recruitment, overnight urine was collected from all participants and stored at -80 degrees C. After an average of 5.5 years of follow-up, 144 breast cancer cases and four matched controls for each case were identified among the participants of the cohort. Among premenopausal women, a higher ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone at baseline was associated with a reduced risk of breast cancer: women in the highest quintile of the ratio had an adjusted odds ratio (OR) for breast cancer of 0.58 [95% confidence interval (CI) = 0.25-1.34]. The corresponding adjusted OR in postmenopausal women was 1.29 (95% CI = 0.53-3.10). Results of this prospective study support the hypothesis that the estrogen metabolism pathway favoring 2-hydroxylation over 16alpha-hydroxylation is associated with a reduced risk of invasive breast cancer risk in premenopausal women
From the studies:
Obesity decreases 2-hydroxyestrone and increases 16-hydroxyestrone production.139,155
Exercise, weight loss, cruciferous vegetables, improve the 2-hydroxyestrone/16-hydroxyestrone ratio, reducing the stimulatory effect on breast tissue.
Dietary consumption of cruciferous vegetables, such as broccoli and cabbage, as well as green tea, garlic, and rosemary can increase the amount of 2-HE by modifying P450 activity in phase I, and have antioxidant effects as well. Which means DIM does produce "catechol estrogens 2-HE by modifying P450 activity" ....that's aromatase.
Altered estrogen metabolism and excretion in humans following consumption of indole‐3‐carbinol
"These results indicate that I3C predictably alters endogenous estrogen metabolism toward increased catechol estrogen production and may thereby provide a novel “dietary”; means for reducing cancer risk"
https://www.tandfonline.com/doi/abs/10.1...9109514141
Catechol estrogens 2-HE by modifying P450 activity
Judging by your comment you didn't look at the posted literature, too bad…I'll list for you again.
DlM improves estrogen metabolism,
DIM shifts production of the dangerous estrogen metabolite 16a-hydroxy in favor of the beneficial (or healthier) 2-hydroxy 2-OH metabolite. So it's hypothesized that the 2 OH pathway over 16α-OH pathway (which is inversely associated with breast cancer risk) is a safer option.
So tell me, can Spiro do all this?
Does Spiro significantly improve insulin resistance like DIM
DIM on human prostate cancer cell growth were examined using LNCaP and PC-3 cells.
Our results showed a concentration-dependent inhibition of DNA synthesis of these cells of up to 90% under both uninduced and androgen-induced growth conditions.
Spiro doesn't even come close to that (60-70% at best)
DIM suppresses cell proliferation of LNCaP cells and inhibits dihydrotestosterone (DHT) stimulation of DNA synthesis.
DIM inhibited androgen-induced androgen receptor (AR) translocation into the nucleus. Results of receptor binding assays indicated further that DIM is a strong competitive inhibitor of DHT binding to the AR.
In addition, DIM inhibited proliferation and induced programmed cell death in human breast tumor cells in culture (20, 21).
We found that DIM is a strong antiandrogen that inhibited androgen-dependent tumor cell growth and competitively inhibited androgen receptor translocation and signal transduction.
DIM disrupts AR function in a manner similar to a chemically dissimilar synthetic antiandrogen, Casodex (similar to Bicalutamide)
(13-11-2014, 05:06 AM)Lotus Wrote: Excess Estrogen (albeit the bad estrogen 16 a-OH and 4-OH) has the potential to get re-absorbed if not properly eliminated through waste and cause cancerous effects, DIM shifts the 2OH-hydroxyestrone over the harmful
16alpha-hydroxylation
Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16alpha-hydroxyestrone ratio in premenopausal and postmenopausal women
P Muti et al. Epidemiology. 2000 Nov.
Show details
Full text links
Cite
Abstract
Experimental and clinical evidence suggests that 16alpha-hydroxylated estrogen metabolites, biologically strong estrogens, are associated with breast cancer risk, while 2-hydroxylated metabolites, with lower estrogenic activity, are weakly related to this disease. This study analyzes the association of breast cancer risk with estrogen metabolism, expressed as the ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone, in a prospective nested case-control study. Between 1987 and 1992, 10,786 women (ages 35-69 years) were recruited to a prospective study on breast cancer in Italy, the "Hormones and Diet in the Etiology of Breast Cancer" (ORDET) study. Women with a history of cancer and women on hormone therapy were excluded at baseline. At recruitment, overnight urine was collected from all participants and stored at -80 degrees C. After an average of 5.5 years of follow-up, 144 breast cancer cases and four matched controls for each case were identified among the participants of the cohort. Among premenopausal women, a higher ratio of 2-hydroxyestrone to 16alpha-hydroxyestrone at baseline was associated with a reduced risk of breast cancer: women in the highest quintile of the ratio had an adjusted odds ratio (OR) for breast cancer of 0.58 [95% confidence interval (CI) = 0.25-1.34]. The corresponding adjusted OR in postmenopausal women was 1.29 (95% CI = 0.53-3.10). Results of this prospective study support the hypothesis that the estrogen metabolism pathway favoring 2-hydroxylation over 16alpha-hydroxylation is associated with a reduced risk of invasive breast cancer risk in premenopausal women
From the studies:
Obesity decreases 2-hydroxyestrone and increases 16-hydroxyestrone production.139,155
Exercise, weight loss, cruciferous vegetables, improve the 2-hydroxyestrone/16-hydroxyestrone ratio, reducing the stimulatory effect on breast tissue.
Dietary consumption of cruciferous vegetables, such as broccoli and cabbage, as well as green tea, garlic, and rosemary can increase the amount of 2-HE by modifying P450 activity in phase I, and have antioxidant effects as well. Which means DIM does produce "catechol estrogens 2-HE by modifying P450 activity" ....that's aromatase.
Altered estrogen metabolism and excretion in humans following consumption of indole‐3‐carbinol
"These results indicate that I3C predictably alters endogenous estrogen metabolism toward increased catechol estrogen production and may thereby provide a novel “dietary”; means for reducing cancer risk"
https://www.tandfonline.com/doi/abs/10.1...9109514141
Catechol estrogens 2-HE by modifying P450 activity